Rifampicin Health Dictionary

Also known as Hansen’s disease, this is a chronic bacterial infection caused by Mycobacterium leprae affecting the skin, mucous membranes, and nerves. Infection is now almost con?ned to tropical and subtropical countries – mostly in Africa and India. There are two distinct (polarised) clinical forms: tuberculoid and lepromatous. The former usually takes a benign course and frequently burns out, whereas the latter is relentlessly progressive; between these two polar forms lies an intermediate/dimorphous group. Susceptibility may be increased by malnutrition. Nasal secretions (especially in lepromatous disease) are teeming with M. leprae and constitute the main source of infection; however, living in close proximity to an infected individual seems necessary for someone to contract the disease. M. leprae can also be transmitted in breast milk from an infected mother.

Only a small minority of those exposed to M. leprae develop the disease. The incubation period is 3–5 years or longer. The major clinical manifestations involve skin and nerves: the former range from depigmented, often anaesthetic areas, to massive nodules; nerve involvement ranges from localised nerve swelling(s) to extensive areas of anaesthesia. Advanced nerve destruction gives rise to severe deformities: foot-drop, wrist-drop, claw-foot, extensive ulceration of the extremities with loss of ?ngers and toes, and bone changes. Eye involvement can produce blindness. Laryngeal lesions produce hoarseness and more serious sequelae. The diagnosis is essentially a clinical one; however, skin-smears, histological features and the lepromin skin-test help to con?rm the diagnosis and enable the form of disease to be graded.

Although the World Health Organisation had originally hoped to eliminate leprosy worldwide by 2000, that has proved an unrealistic target. The reason is an absence of basic information. Doctors are unable to diagnose the disorder before a patient starts to show symptoms; meanwhile he or she may have already passed on the infection. Doctors do not know exactly how transmission occurs or how it infects humans – nor do they know at what point a carrier of the bacterium may infect others. The incidence of new infections is still more than 650,000 cases a year or about 4.5 cases per 10,000 people in those countries worst affected by the disease.

Treatment Introduction of the sulphone compound, dapsone, revolutionised management of the disease. More recently, rifampicin and clofazimine have been added as ?rst-line drugs for treatment. Second-line drugs include minocycline, o?oxacin and clarithromycin; a number of regimens incorporating several of these compounds (multi-drug regimens – introduced in 1982) are now widely used. A three-drug regime is recommended for multi-bacillary leprosy and a two-drug one for parcibacillary leprosy. Dapsone resistance is a major problem worldwide, but occurs less commonly when multi-drug regimens are used. Older compounds – ethionamide and prothionamide

– are no longer used because they are severely toxic to the liver. Corticosteroids are sometimes required in patients with ‘reversal reaction’. Supportive therapy includes physiotherapy; both plastic and orthopaedic surgery may be necessary in advanced stages of the disease. Improvement in socio-economic conditions, and widespread use of BCG vaccination are of value as preventive strategies. Early diagnosis and prompt institution of chemotherapy should prevent long-term complications.... leprosy

An infectious disease, commonly called , caused in humans by the bacterium MYCOBACTERIUM TUBERCULOSIS. is usually transmitted in airborne droplets expelled when an infected person coughs or sneezes. An inhaled droplet enters the lungs and the bacteria begin multiplying. The immune system usually seals off the infection at this point, but in about 5 per cent of cases the infection spreads to the lymph nodes. It may also spread to other organs through the bloodstream, which may lead to miliary tuberculosis, a potentially fatal form of the disease.

In about another 5 per cent of cases, bacteria held in a dormant state by the immune system become reactivated months, or even years, later. The infection may then progressively damage the lungs, forming cavities.

The primary infection is usually without symptoms. Progressive infection in the lungs causes coughing (sometimes bringing up blood), chest pain, shortness of breath, fever and sweating, poor appetite, and weight loss. Pleural effusion or pneumothorax may develop. The lung damage may be fatal.

A diagnosis is made from the symptoms and signs, from a chest X-ray, and from tests on the sputum. Alternatively, a bronchoscopy may also be carried out to obtain samples for culture.

Treatment is usually with a course of 3 or 4 drugs, taken daily for 2 months, followed by daily doses of isoniazid and rifampicin for 4–6 months. However, bacteria are increasingly resistant to the drugs used in treatment, and others may have to be used and treatment carried out for a longer period. If the full course of drugs is taken, most patients recover.

can be prevented by BCG vaccination, which is offered routinely at birth or age 10–14.

Any contacts of an infected person are traced and examined, and, if infected, are treated early to reduce the risk of the infection spreading.... tuberculosis

In?ammation of the LIVER which damages liver cells and may ultimately kill them. Acute injury of the liver is usually followed by complete recovery, but prolonged in?ammation after injury may result in FIBROSIS and CIRRHOSIS. Excluding trauma, hepatitis has several causes:

Viral infections by any of hepatitis A, B, C, D, or E viruses and also CYTOMEGALOVIRUS (CMV), EPSTEIN BARR VIRUS, and HERPES SIMPLEX.

Autoimmune disorders such as autoimmune chronic hepatitis, toxins, alcohol and certain drugs – ISONIAZID, RIFAMPICIN, HALOTHANE and CHLORPROMAZINE.

WILSON’S DISEASE.

Acute viral hepatitis causes damage throughout the liver and in severe infections may destroy whole lobules (see below).

Chronic hepatitis is typi?ed by an invasion of the portal tract by white blood cells (mild hepatitis). If these mononuclear in?ammatory cells invade the body (parenchyma) of the liver tissue, ?brosis and then chronic disease or cirrhosis can develop. Cirrhosis may develop at any age and commonly results in prolonged ill health. It is an important cause of premature death, with excessive alcohol consumption commonly the triggering factor. Sometimes, cirrhosis may be asymptomatic, but common symptoms are weakness, tiredness, poor appetite, weight loss, nausea, vomiting, abdominal discomfort and production of abnormal amounts of wind. Initially, the liver may enlarge, but later it becomes hard and shrunken, though rarely causing pain. Skin pigmentation may occur along with jaundice, the result of failure to excrete the liver product BILIRUBIN. Routine liver-function tests on blood are used to help diagnose the disease and to monitor its progress. Spider telangiectasia (caused by damage to blood vessels – see TELANGIECTASIS) usually develop, and these are a signi?cant pointer to liver disease. ENDOCRINE changes occur, especially in men, who lose their typical hair distribution and suffer from atrophy of their testicles. Bruising and nosebleeds occur increasingly as the cirrhosis worsens, and portal hypertension (high pressure of venous blood circulation through the liver) develops due to abnormal vascular resistance. ASCITES and HEPATIC ENCEPHALOPATHY are indications of advanced cirrhosis.

Treatment of cirrhosis is to tackle the underlying cause, to maintain the patient’s nutrition (advising him or her to avoid alcohol), and to treat any complications. The disorder can also be treated by liver transplantation; indeed, 75 per cent of liver transplants are done for cirrhosis. The overall prognosis of cirrhosis, however, is not good, especially as many patients attend for medical care late in the course of the disease. Overall, only 25 per cent of patients live for ?ve years after diagnosis, though patients who have a liver transplant and survive for a year (80 per cent do) have a good prognosis.

Autoimmune hepatitis is a type that most commonly occurs in women between 20 and 40 years of age. The cause is unknown and it has been suggested that the disease has several immunological subtypes. Symptoms are similar to other viral hepatitis infections, with painful joints and AMENORRHOEA as additional symptoms. Jaundice and signs of chronic liver disease usually occur. Treatment with CORTICOSTEROIDS is life-saving in autoimmune hepatitis, and maintenance treatment may be needed for two years or more. Remissions and exacerbations are typical, and most patients eventually develop cirrhosis, with 50 per cent of victims dying of liver failure if not treated. This ?gure falls to 10 per cent in treated patients.

Viral hepatitis The ?ve hepatic viruses (A to E) all cause acute primary liver disease, though each belongs to a separate group of viruses.

•Hepatitis A virus (HAV) is an ENTEROVIRUS

which is very infectious, spreading by faecal contamination from patients suffering from (or incubating) the infection; victims excrete viruses into the faeces for around ?ve weeks during incubation and development of the disease. Overcrowding and poor sanitation help to spread hepatitis A, which fortunately usually causes only mild disease.

Hepatitis B (HBV) is caused by a hepadna virus, and humans are the only reservoir of infection, with blood the main agent for transferring it. Transfusions of infected blood or blood products, and injections using contaminated needles (common among habitual drug abusers), are common modes of transfer. Tattooing and ACUPUNCTURE may spread hepatitis B unless high standards of sterilisation are maintained. Sexual intercourse, particularly between male homosexuals, is a signi?cant infection route.

Hepatitis C (HCV) is a ?avivirus whose source of infection is usually via blood contacts. E?ective screening of blood donors and heat treatment of blood factors should prevent the spread of this infection, which becomes chronic in about 75 per cent of those infected, lasting for life. Although most carriers do not suffer an acute illness, they must practise life-long preventive measures.

Hepatitis D (HDV) cannot survive independently, needing HBV to replicate, so its sources and methods of spread are similar to the B virus. HDV can infect people at the same time as HBV, but it is capable of superinfecting those who are already chronic carriers of the B virus. Acute and chronic infection of HDV can occur, depending on individual circumstances, and parenteral drug abuse spreads the infection. The disease occurs worldwide, being endemic in Africa, South America and the Mediterranean littoral.

Hepatitis E virus (HEV) is excreted in the stools, spreading via the faeco-oral route. It causes large epidemics of water-borne hepatitis and ?ourishes wherever there is poor sanitation. It resembles acute HAV infection and the patient usually recovers. HEV does not cause chronic infection. The clinical characteristics of the ?ve hepatic

viruses are broadly similar. The initial symptoms last for up to two weeks (comprising temperature, headache and malaise), and JAUNDICE then develops, with anorexia, nausea, vomiting and diarrhoea common manifestations. Upper abdominal pain and a tender enlarged liver margin, accompanied by enlarged cervical lymph glands, are usual.

As well as blood tests to assess liver function, there are speci?c virological tests to identify the ?ve infective agents, and these are important contributions to diagnosis. However, there is no speci?c treatment of any of these infections. The more seriously ill patients may require hospital care, mainly to enable doctors to spot at an early stage those developing acute liver failure. If vomiting is a problem, intravenous ?uid and glucose can be given. Therapeutic drugs – especially sedatives and hypnotics – should be avoided, and alcohol must not be taken during the acute phase. Interferon is the only licensed drug for the treatment of chronic hepatitis B, but this is used with care.

Otherwise-?t patients under 40 with acute viral hepatitis have a mortality rate of around

0.5 per cent; for those over 60, this ?gure is around 3 per cent. Up to 95 per cent of adults with acute HBV infection recover fully but the rest may develop life-long chronic hepatitis, particularly those who are immunode?cient (see IMMUNODEFICIENCY).

Infection is best prevented by good living conditions. HVA and HVB can be prevented by active immunisation with vaccines. There is no vaccine available for viruses C, D and E, although HDV is e?ectively prevented by immunisation against HBV. At-risk groups who should be vaccinated against HBV include:

Parenteral drug abusers.

Close contacts of infected individuals such as regular sexual partners and infants of infected mothers.

Men who have sex with men.

Patients undergoing regular haemodialysis.

Selected health professionals, including laboratory sta? dealing with blood samples and products.... hepatitis

One of the anti-tuberculous drugs. It has the advantages of being relatively non-toxic and of being active when taken by mouth. Unfortunately, like streptomycin, it may render the Mycobacterium tuberculosis resistant to its action. This tendency to produce resistance is considerably reduced if it is given in conjunction with RIFAMPICIN and PYRAZINAMIDE.... isoniazid

A form of PNEUMONIA due to a bacterium known as Legionella pneumophila, so-called because the ?rst identi?ed outbreak was in a group of US ex-servicemen (members of the American Legion). Inhalation of water aerosols seems the most likely way that people acquire the disease, for example from air-conditioning outlets. Some rubber outlets in showers and taps are able to support the growth of legionnellae so that high concentrations of the organism are released when the tap is ?rst used in the morning. In the presence of the disease, the treatment of infected water systems is essential by cleaning, chlorination, heating or a combination of all three.

The pneumonia caused by legionnellae has no distinctive clinical or radiological features, so that the diagnosis is based on an antibody test performed on a blood sample. There is no evidence that the disease is transmitted directly from person to person. The incubation period is 2–10 days; the disease starts with aches and pains followed rapidly by a rise in temperature, shivering attacks, cough and shortness of breath. The X-ray tends to show patchy areas of consolidation in the lungs. Erythromycin and rifampicin are the most useful antibiotics, although rifampicin should never be given alone because of the rapid development of drug resistance.... legionnaire’s disease

One of the early antituberculous (see TUBERCULOSIS) antibiotics. It tended to cause DYSPEPSIA and has been replaced by newer antituberculous drugs with fewer side-effects. The ?rst-line drugs for tuberculosis are now rifampicin, isoniazid, and ethambutol.... para-amino salicylic acid

An antituberculous drug used in combination, usually with RIFAMPICIN and ISONIAZID, as the treatment regime for TUBERCULOSIS. It penetrates the MENINGES so is valuable in treating tuberculous MENINGITIS. The drug is sometimes associated with liver damage and liver function tests should be done before using it.... pyrazinamide

In?ammation affecting the membranes of the BRAIN or SPINAL CORD, or usually both. Meningitis may be caused by BACTERIA, viruses (see VIRUS), fungi, malignant cells or blood (after SUBARACHNOID HAEMORRHAGE). The term is, however, usually restricted to in?ammation due to a bacterium or virus. Viral meningitis is normally a mild, self-limiting infection of a few days’ duration; it is the most common cause of meningitis but usually results in complete recovery and requires no speci?c treatment. Usually a less serious infection than the bacterial variety, it does, however, rarely cause associated ENCEPHALITIS, which is a potentially dangerous illness. A range of viruses can cause meningitis, including: ENTEROVIRUSES; those causing MUMPS, INFLUENZA and HERPES SIMPLEX; and HIV.

Bacterial meningitis is life-threatening: in the United Kingdom, 5–10 per cent of children who contract the disease may die. Most cases of acute bacterial meningitis in the UK are caused by two bacteria: Neisseria meningitidis (meningococcus), and Streptococcus pneumoniae (pneumococcus); other bacteria include Haemophilus in?uenzae (a common cause until virtually wiped out by immunisation), Escherichia coli, Mycobacterium tuberculosis (see TUBERCULOSIS), Treponema pallidum (see SYPHILIS) and Staphylococci spp. Of the bacterial infections, meningococcal group B is the type that causes a large number of cases in the UK, while group A is less common.

Bacterial meningitis may occur by spread from nearby infected foci such as the nasopharynx, middle ear, mastoid and sinuses (see EAR, DISEASES OF). Direct infection may be the result of penetrating injuries of the skull from accidents or gunshot wounds. Meningitis may also be a complication of neurosurgery despite careful aseptic precautions. Immuno-compromised patients – those with AIDS or on CYTOTOXIC drugs – are vulnerable to infections.

Spread to contacts may occur in schools and similar communities. Many people harbour the meningococcus without developing meningitis. In recent years small clusters of cases, mainly in schoolchildren and young people at college, have occurred in Britain.

Symptoms include malaise accompanied by fever, severe headache, PHOTOPHOBIA, vomiting, irritability, rigors, drowsiness and neurological disturbances. Neck sti?ness and a positive KERNIG’S SIGN appearing within a few hours of infection are key diagnostic signs. Meningococcal and pneumococcal meningitis may co-exist with SEPTICAEMIA, a much more serious condition in terms of death rate or organ damage and which constitutes a grave emergency demanding rapid treatment.

Diagnosis and treatment are urgent and, if bacterial meningitis is suspected, antibiotic treatment should be started even before laboratory con?rmation of the infection. Analysis of the CEREBROSPINAL FLUID (CSF) by means of a LUMBAR PUNCTURE is an essential step in diagnosis, except in patients for whom the test would be dangerous as they have signs of raised intracranial pressure. The CSF is clear or turbid in viral meningitis, turbid or viscous in tuberculous infection and turbulent or purulent when meningococci or staphylococci are the infective agents. Cell counts and biochemical make-up of the CSF are other diagnostic pointers. Serological tests are done to identify possible syphilitic infection, which is now rare in Britain.

Patients with suspected meningitis should be admitted to hospital quickly. General pracitioners are encouraged to give a dose of intramuscular penicillin before sending the child to hospital. Treatment in hospital is usually with a cephalosporin, such as ceftazidime or ceftriaxone. Once the sensitivity of the organism is known as a result of laboratory studies on CSF and blood, this may be changed to penicillin or, in the case of H. in?uenzae, to amoxicillin. Local infections such as SINUSITIS or middle-ear infection require treatment, and appropriate surgery for skull fractures or meningeal tears should be carried out as necessary. Tuberculous meningitis is treated for at least nine months with anti-tuberculous drugs (see TUBERCULOSIS). If bacterial meningitis causes CONVULSIONS, these can be controlled with diazepam (see TRANQUILLISERS; BENZODIAZEPINES) and ANALGESICS will be required for the severe headache.

Coexisting septicaemia may require full intensive care with close attention to intravenous ?uid and electrolyte balance, control of blood clotting and blood pressure.

Treatment of close contacts such as family, school friends, medical and nursing sta? is recommended if the patient has H. in?uenzae or N. meningitidis: RIFAMPICIN provides e?ective prophylaxis. Contacts of patients with pneumococcal infection do not need preventive treatment. Vaccines for meningococcal meningitis may be given to family members in small epidemics and to any contacts who are especially at risk such as infants, the elderly and immuno-compromised individuals.

The outlook for a patient with bacterial meningitis depends upon age – the young and old are vulnerable; speed of onset – sudden onset worsens the prognosis; and how quickly treatment is started – hence the urgency of diagnosis and admission to hospital. Recent research has shown that children who suffer meningitis in their ?rst year of life are ten times more likely to develop moderate or severe disability by the age of ?ve than contemporaries who have not been infected. (See British Medical Journal, 8 September 2001, page 523.)

Prevention One type of bacterial meningitis, that caused by Haemophilus, has been largely controlled by IMMUNISATION; meningococcal C vaccine has largely prevented this type of the disease in the UK. So far, no vaccine against group B has been developed, but research continues. Information on meningitis can be obtained from the Meningitis Trust and the Meningitis Research Foundation.... meningitis

Most staphylococci (see STAPHYLOCOCCUS) have now evolved resistance to benzylpenicillin (see PENICILLIN) because of their ability to produce PENICILLINASE. Cloxacillin and ?ucloxacillin are antibiotics still e?ective against most staphylococci; at one time methicillin was used to combat resistant strains, but in hospital environments bacteria acquired immunity to this powerful drug (now withdrawn from use) and to cloxacillin. RIFAMPICIN, VANCOMYCIN, TEICOPLANIN and temocillin are still active against most penicillinase-producing gram-negative bacteria (see GRAM’S STAIN). There is, however, a growing threat to health because of the rise in the number of antibiotic-resistant bacteria, particularly in hospitals. The bacteria themselves are not more virulent than others, but the di?culty in treating them with a safe and e?ective antibiotic mean that they are more dangerous. It is likely that lapses in normal hygienic practice – such as frequent hand-washing – has resulted in an increase in MRSA disease.... methicillin-resistant staphylococcus aureus (mrsa)

been recognised from earliest times. Evidence of the condition has been found in Egyptian mummies; in the fourth century BC Hippocrates, the Greek physician, called it phthisis because of the lung involvement; and in 1882 Koch announced the discovery of the causative organism, the tubercle bacillus or Mycobacterium tuberculosis.

The symptoms depend upon the site of the infection. General symptoms such as fever, weight loss and night sweats are common. In the most common form of pulmonary tuberculosis, cough and blood-stained sputum (haemoptysis) are common symptoms.

The route of infection is most often by inhalation, although it can be by ingestion of products such as infected milk. The results of contact depend upon the extent of the exposure and the susceptibility of the individual. Around 30 per cent of those closely exposed to the organism will be infected, but most will contain the infection with no signi?cant clinical illness and only a minority will go on to develop clinical disease. Around 5 per cent of those infected will develop post-primary disease over the next two or three years. The rest are at risk of reactivation of the disease later, particularly if their resistance is reduced by associated disease, poor nutrition or immunosuppression. In developed countries around 5 per cent of those infected will reactivate their healed tuberculosis into a clinical problem.

Immunosuppressed patients such as those infected with HIV are at much greater risk of developing clinical tuberculosis on primary contact or from reactivation. This is a particular problem in many developing countries, where there is a high incidence of both HIV and tuberculosis.

Diagnosis This depends upon identi?cation of mycobacteria on direct staining of sputum or other secretions or tissue, and upon culture of the organism. Culture takes 4–6 weeks but is necessary for di?erentiation from other non-tuberculous mycobacteria and for drug-sensitivity testing. Newer techniques involving DNA ampli?cation by polymerase chain reaction (PCR) can detect small numbers of organisms and help with earlier diagnosis.

Treatment This can be preventative or curative. Important elements of prevention are adequate nutrition and social conditions, BCG vaccination (see IMMUNISATION), an adequate public-health programme for contact tracing, and chemoprophylaxis. Radiological screening with mass miniature radiography is no longer used.

Vaccination with an attenuated organism (BCG – Bacillus Calmette Guerin) is used in the United Kingdom and some other countries at 12–13 years, or earlier in high-risk groups. Some studies show 80 per cent protection against tuberculosis for ten years after vaccination.

Cases of open tuberculosis need to be identi?ed; their close contacts should be reviewed for evidence of disease. Adequate antibiotic chemotherapy removes the infective risk after around two weeks of treatment. Chemoprophylaxis – the use of antituberculous therapy in those without clinical disease – may be used in contacts who develop a strong reaction on tuberculin skin testing or those at high risk because of associated disease.

The major principles of antibiotic chemotherapy for tuberculosis are that a combination of drugs needs to be used, and that treatment needs to be continued for a prolonged period – usually six months. Use of single agents or interrupted courses leads to the development of drug resistance. Serious outbreaks of multiply resistant Mycobacterium tuberculosis have been seen mainly in AIDS units, where patients have greater susceptibility to the disease, but also in developing countries where maintenance of appropriate antibacterial therapy for six months or more can be di?cult.

Streptomycin was the ?rst useful agent identi?ed in 1944. The four drugs used most often now are RIFAMPICIN, ISONIAZID, PYRAZINAMIDE and ETHAMBUTOL. Three to four agents are used for the ?rst two months; then, when sensitivities are known and clinical response observed, two drugs, most often rifampicin and isoniazid, are continued for the rest of the course. Treatment is taken daily, although thrice-weekly, directly observed therapy is used when there is doubt about the patient’s compliance. All the antituberculous agents have a range of adverse effects that need to be monitored during treatment. Provided that the treatment is prescribed and taken appropriately, response to treatment is very good with cure of disease and very low relapse rates.... nature of the disease tuberculosis has

Bennett.

Family: Simaroubaceae.

Habitat: Garhwal, Himachal Pradesh and Kulu.

English: Quassia (substitute for P excelsa Lindtl).

Ayurvedic: Bhurangi, Nimbi. (Clerodendrum serratum and its related species represent Bhaargi or Bhaarangi.)

Folk: Nimatotaa.

Action: Wood—a non-astringent bitter tonic and stomachic, amoe- bicidal, anthelmintic (used as enema), insect repellent. Used as a supporting medicine for temporary relief in cirrhosis of liver.

Many indole alkaloids of beta-car- boline, canthin-6-one and beta-carbo- line dimer type, have been isolated from the wood. These are reported to increase the blood flow rate in the intestine and stomach of rabbit; also exhibited antiviral activity on Herpes simplex virus.

Nigaki lactone and methylnigaki- none, isolated from the wood, showed antigastric ulcer activity in rats. The extract of the wood is reported to prevent the secretion of gastric juice in a dose-dependent manner in rats. The extract also showed the same effects on rats having aspirin-induced gastric ulcer.

Family: Scrophulariaceae.

Habitat: The alpine Himalayas from Kashmir to Sikkim.

English: Picrorhiza.

Ayurvedic: Katukaa, Katurohini, Kattarohini, Katuki, Katukikaa, Krishnabhedaa, Kaandaruhaa, Matsyashakalaa, Chakraangi, Shat- parvaa, Arishta, Ashokarohinya, Shakuldaani.

Unani: Kutki, Kharbaq-e-Hindi.

Siddha/Tamil: Kaduguragini.

Action: Root—stomachic, antidiar- rhoeal, cholagogue, hepatoprotec- tive. Used in hepatitis, chronic dysentery, amoebiasis.

Key application: In jaundice, intermittent fever, dyspnoea and skin diseases. (The Ayurvedic Pharmacopoeia ofIndia.)

The roots yield a glycosidal bitter principle, kutkin, found to be a mixture of two iridoid glycosides, picro- side I and kutkoside. Also obtained were D-mannitol, kutkiol, kutkisterol and a ketone (identical with apocynin).

Kutkin exhibited hepatoprotective activity in CCl4-induced toxic rats.

Picroliv, a standardized fraction from the alcoholic extract of the root and rhizome, containing 55-60% of a mixture of picroside I and kutkoside (1:15) showed dose-dependent protective activity on isolated hepatocytes in vitro against thiocetamide-induced hepatic damage in rat and was found to be more potent than Silymarin, a known hepatoprotective agent. Pi- croliv is reported to show protective effect against rifampicin-induced hep- atotoxicity in rats. It also exerts hy- polipidaemic effect in normal, triton- treated and cholesterol-fed rats.

Kutkin, picroside I and kutkoside exhibit anti-inflammatory property.

The phenolic glycoside, androsin, isolated from the plant, prevents allergen and platelet activating factor- induced bronchial obstruction in guinea-pigs in vitro.

Cucurbitacin glycosides, isolated from the root, exhibit liver protective, tumour inhibitory and anti-inflammatory activity.

Dosage: Root—1-3 g; 3-6 g as purgative. (CCRAS.)... picrasma quassioides

A chronic bacterial infection, also called leprosy, that damages nerves, mainly in the limbs and facial area, and may cause skin damage. The disease is caused by a bacterium,MYCOBACTERIUM LEPRAE, which is spread in droplets of nasal mucus. Hansen’s disease is not highly contagious, and a person is infectious only in the early stages. Prolonged close contact puts people at risk. The disease is most prevalent in Asia, Central America, South America, and Africa.

Hansen’s disease has a long incubation period – about 3–5 years. There are 2 main types: the lepromatous type, in which damage is widespread, progressive, and severe; and the tuberculoid type, which is milder. In both types, damage is initially confined to peripheral nerves supplying the skin and muscles. Skin areas supplied by affected nerves become lighter or darker and sensation and sweating are reduced. As the disease progresses, the peripheral nerves swell and become tender. Hands, feet, and facial skin eventually become numb and muscles become paralysed, leading to deformity. Other possible features include blindness, destruction of bone, and sterility.

The presence of the causative bacteria is confirmed by a skin biopsy. Drug treatment may be with a combination of dapsone, rifampicin, and clofazimine, which kills most of the bacteria in a few days. Any damage that has occurred before treatment, however, is irreversible. Plastic surgery may be necessary to correct deformities; and nerve and tendon transplants may improve the function of damaged limbs.... hansen’s disease